While the relationship between laboratory responses to acute psychosocial stressors and cardiovascular function has been explored for decades, only recently have researchers become interested in examining the additional impact of such stressors on immune function. Brief laboratory stressors have been shown to induce significant increases in some parameters of cell-mediated immunity. Interestingly, these stress-related immunologic changes appear to be potentiated in individuals who are also strong cardiovascular reactors to stress. In other words, those individuals who show the greatest cardiovascular response to brief psychological stressors also exhibit increased enhancement of functions that contribute to the cell-mediated immune response. Despite these interesting findings, acute laboratory-induced stressors have yet to be correlated significantly with clinically relevant shifts in the cell-mediated immune response. This is the primary objective of the proposed research project, which would be undertaken using the delayed-type hypersensitivity (DTH) response as a clinically relevant model of cell-mediated immunity. Subjects would be required to complete two separate experimental sessions (baseline vs. acute stress), spaced two weeks apart, which would be counterbalanced. Injection of tetanus toxoid at the end of each session would serve to initiate the DTH response, and subjects would be required to return 48 hours after each of the experimental sessions so that the magnitude of these DTH responses could be assessed. The acute stressor would be a simulated public speaking task. Heart rate, stroke volume, pre-ejection period and left ventricular ejection time would be measured continuously and non-invasively during the two experimental sessions using impedance cardiographic techniques, and blood pressure would be monitored at regular intervals using an automated blood pressure monitor. It is hypothesized that DTH responses that are initiated immediately following the stressful task will be significantly larger in magnitude than DTH responses initiated during the baseline condition, and that stress-induced enhancement of the DTH response will be directly related to stress-induced cardiovascular reactivity.